Practicals Term I (+BP Prac) Flashcards
Gram +ve bacteria
- have thick peptidoglycan cell walls
- stain purple/blue
- like dry environments
Gram +ve cocci on Gram stain suggest
normal flora
Gram -ve bacteria
- have thin peptidoglycan cell walls and an outer membrane
- do not stain (ie pink or red)
- like moist environments
Gram +ve clusters are
Staphylococci
Gram +ve chains are
Streptococci
Green pus is likely caused by
Pseudomonas aeruginosa
Sulphur granules in pus indicate
Actinomyces israelii
Pus with an offensive odour is likely caused by
anaerobes
Thick, yellow pus is likely caused by
Staphylococcus aureus, etc.
Genetics account for what percent of BP variation in the population?
40%
What happens to systolic BP on sitting??
drops slightly; then restored (but not to lying pressure)
What happens to SV on sitting from lying?
- decreases
- perceived as a slight drop in BP by baroreceptors in carotids and aorta as decreased stretch
- baroreceptors fire to activate medulla to increase SNS tone and decreased PNS tone
- increased SNS and decreased PS increase HR and contractility to restore SV(but not to same level as lying)
What happens to systolic BP on standing from sitting?
initial drop in BP; restored
What happens to SV on standing from sitting?
drops; activates +SNS and -PNS via baroreceptor reflex to increase HR and restore SV
What happens to HR from lying to standing?
increases
What happens to diastolic BP from lying to standing?
decreases
What happens to cardiac output from lying to standing?
decreases
What happens to total peripheral resistance from lying to standing?
decreases
How does the body increase MAP from lying to standing?
by increasing TPR
(inc HR would compromise diastolic filling of coronaries)
Nicotine
increases BP, HR
Caffiene
initially increases blood pressure, long-term effects unknown
What are primary immunodeficiencies?
- result of inherent congenital defects in the components of the immune system or their products
What are secondary immunodeficiencies?
- result from effects of external agents or alterations in other body systems
- more common than primary
- associated with:
- extremes of age
- malnutrition
- anatomic barrier dysfunction (incl medical devices)
- non-infectious diseases (diabetes, tumours/cancer)
- infections (malaria, HIV)
- cytotoxic drugs/irradiation (chemo)
- immunosuppresive drugs
Secondary immunodeficiencies are associated with
- extremes of age
- malnutrition
- anatomic barrier dysfunction (incl medical devices)
- non-infectious diseases (diabetes, tumours/cancer)
- infections (malaria, HIV)
- cytotoxic drugs/irradiation (chemo)
- immunosuppresive drugs
Recessive gene defects that cause primary immunodeficiencies include
- defects in development of primary lymphoid tissue (thymus, spleen)
- defects in T cell development
- MHC Class I or II deficiency
- defects in B cell development and selected antibody deficiencies
- phagocyte deficiencies
- complement pathway deficiencies
What blood specimens are collected for immunodeficiency diagnosis?
- blood - anticoagulant:
- # s and function of immune cells
- blood - plain tube:
- clots; for complement and antibody estimations
What is the order of isotype switching?
IgM > IgG > IgE > IgA
How is blood analysed for populations of lymphocytes?
flow cytometry using anti-T (anti-CD3) and anti-B (anti-CD19) cell antibodies as markers
How are lymphocytes analysed in the blood?
- flow cytometry for populations using anti-T (anti-CD3) and anti-B (anti-CD19) cell antibodies
- antibody isotype analysis (IgG, IgM, IgE, IgA)
- specific antibody analysis (tetanus, blood groups)
- t-cell proliferation tests
- flow cytometry of CD40L expression on activated lymphocytes